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   <subfield code="a">MnTMPyP, a superoxide dismutase/catalase mimetic, decreases inflammatory indices in ischemic acute kidney injury</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Jordan Mortensen, Brian Shames, Christopher Johnson, Vani Nilakantan]</subfield>
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   <subfield code="a">Objective: This study investigates the effect of a superoxide dismutase mimetic, MnTMPyP, on pro- and anti-inflammatory cytokines in acute renal ischemia-reperfusion (IR). Materials and treatment: Male Sprague-Dawley rats underwent bilateral clamping of the renal arteries for 45min followed by 1, 4, or 24h of reperfusion. A subset of animals was treated with MnTMPyP (5mg/kg, i.p.) or saline. Porcine proximal tubular epithelial cells were ATP-depleted for 4h followed by recovery for 2h. Methods: Cytokines were analyzed by ELISA, and ED1+ macrophages and CD8+ T lymphocytes by immunohistochemistry. Statistical analysis was performed using ANOVA. Results: MnTMPyP attenuated the IR-mediated increase in serum creatinine and circulating levels of interleukin (IL)-2 following 24h of reperfusion. Furthermore, treatment attenuated increases in tissue levels of tumor necrosis factor (TNF)-α, IL-2, IL-4, and IL-13. MnTMPyP partially prevented the IR-induced infiltration of ED1+ macrophages and CD8+ T lymphocytes in the kidney. ATP depletion-recovery of porcine proximal tubular epithelial cells resulted in decreased IL-6 and IL-10 levels, and MnTMPyP partially restored these cytokines. Conclusions: These results show that MnTMPyP is partially effective in reducing inflammation associated with renal IR and that reactive oxygen species play a role in modulating both pro- and anti-inflammatory pathways in acute kidney injury.</subfield>
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